Journal of Andrology
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Published-Ahead-of-Print July 26, 2006, DOI:10.2164/jandrol.106.000448

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Effects of estradiol infusion in GnRH immunized boars on spermatogenesis

Anna Wagner , Nina Messe , Martin Bergmann , Oksana Lekhkota , and Rolf Claus *

* To whom correspondence should be addressed. E-mail: thsekret{at}uni-hohenheim.de.

Active immunization of boars against GnRH inhibits LH and testicular steroids, so that mitosis of spermatogonia is reduced and apoptosis increased. To clarify whether high amounts of estrogens which are synthesized in the boar testis support spermatogenesis, a group of 6 boars was immunized against GnRH and then infused for seven weeks with estradiol (E2-17{beta}). For comparison, intact boars and immunized boars were infused with saline only. Testicular tissue was then analysed by immunocytochemistry for apoptosis (Tunel, EM), mitosis (Ki67) and estrogen receptor alpha (ER{alpha}). The specifity of ER{alpha} staining was confirmed by RT-PCR and western blot. Immunization decreased LH and testosterone to minimal concentrations in immunized and E217{beta} infused immunized boars whereas FSH was not significantly altered. Estradiol decreased to base levels after immunization. Infusion increased E2-17{beta} in peripheral blood plasma of the immunized boars to physiological levels. Except A-spermatogonia all spermatogenic cells decreased after immunization by about 60%. After estradiol infusion, cell counts increased again and were intermediate between control and immunized boars. Mitosis of spermatogonia was reduced by nearly 50% due to immunization but was partly restored by E2-17{beta} infusion. Expression of ER{alpha} was localized in spermatogonia, suggesting stimulation of mitosis which was further confirmed due to its predominant occurence in stage I of the seminiferous epithelial cycle (main stage of cell division). Apoptosis was minimal in boars but elevated in the other two groups. Data show that estrogens in physiological concentrations support mitosis, but are not sufficient to normalize sperm production because apoptosis was still high.


Key words: estrogen receptor • spermatogenic stage • mitosis • apoptosis






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